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Chapter 6 : Molecular Mimicry and Heart Disease
Heart diseases are the most prevalent cause of morbidity and mortality in rich countries. A common cause of progressive heart disease, heart failure, and sudden death is dilated cardiomyopathy (DCM), a group of disorders in which the heart muscle is weakened and cannot pump effectively. Chlamydia infections, in particular, are epidemiologically linked to human heart disease. Chlamydia infections cause pneumonia and conjunctivitis in children and are a primary cause of sexually transmitted diseases and female infertility. The development of a murine model of autoimmune myocarditis was based on genetic differences among inbred mouse strains in the immune response to CVB3-induced myocarditis. Experimental induction of most autoimmune diseases requires CD4+ T-helper cells responsive to the self-antigen presented on major histocompatability complex (MHC) class II molecules, and administration of monoclonal antibodies (MAbs) against CD4 molecules can block disease in experimental and genetic animal models of autoimmunity. Hence, CD4+ T-helper lymphocytes appear to be crucial regulators for the initiation of T-cell-dependent autoimmunity, and clinical trials that target the CD4+ cell lineage are under way in an examination of treatments for various human autoimmune diseases. Chronic heart diseases in humans have been linked to certain HLA alleles, such as HLA-DQ6. Experimental in vivo and in vitro data provide evidence of molecular mimicry between bacterial antigens and heart-specific proteins and indicate that bacterial peptides can trigger tissue-specific inflammation of the heart. After initiation of the inflammatory process by CD4+ T cells, CD8+ cells and macrophages are recruited into the heart muscle and contribute to disease pathogenesis.